Microarray and real-time RT-PCR analyses of differential human gene expression patterns induced by severe acute respiratory syndrome (SARS) coronavirus infection of Vero cells.
Identifieur interne : 002836 ( PubMed/Corpus ); précédent : 002835; suivant : 002837Microarray and real-time RT-PCR analyses of differential human gene expression patterns induced by severe acute respiratory syndrome (SARS) coronavirus infection of Vero cells.
Auteurs : W F Leong ; H C Tan ; E E Ooi ; D R Koh ; Vincent T K. ChowSource :
- Microbes and infection [ 1286-4579 ] ; 2005.
English descriptors
- KwdEn :
- MESH :
- genetics : Genes, Viral.
- metabolism : Severe Acute Respiratory Syndrome.
- physiology : Genes, Viral, SARS Virus.
- Animals, Chlorocebus aethiops, Gene Expression Profiling, Gene Expression Regulation, Humans, Reverse Transcriptase Polymerase Chain Reaction, Vero Cells.
Abstract
Vero E6 African green monkey kidney cells are highly susceptible to infection with the newly emerging severe acute respiratory syndrome coronavirus (SARS-CoV), and they are permissive for rapid viral replication, with resultant cytopathic effects. We employed cDNA microarray analysis to characterize the cellular transcriptional responses of homologous human genes at 12 h post-infection. Seventy mRNA transcripts belonging to various functional classes exhibited significant alterations in gene expression. There was considerable induction of heat shock proteins that are crucial to the immune response mechanism. Modified levels of several transcripts involved in pro-inflammatory and anti-inflammatory processes exemplified the balance between opposing forces during SARS pathogenesis. Other genes displaying altered transcription included those associated with host translation, cellular metabolism, cell cycle, signal transduction, transcriptional regulation, protein trafficking, protein modulators, and cytoskeletal proteins. Alterations in the levels of several novel transcripts encoding hypothetical proteins and expressed sequence tags were also identified. In addition, transcription of apoptosis-related genes DENN and hIAP1 was upregulated in contrast to FAIM. Elevated Mx1 expression signified a strong host response to mediate antiviral resistance. Also expressed in infected cells was the C-terminal alternative splice variant of the p53 tumor suppressor gene encoding a modified truncated protein that can influence the activity of wild-type p53. We observed the interplay between various mechanisms to favor virus multiplication before full-blown apoptosis and the triggering of several pathways in host cells in an attempt to eliminate the pathogen. Microarray analysis identifies the critical host-pathogen interactions during SARS-CoV infection and provides new insights into the pathophysiology of SARS.
DOI: 10.1016/j.micinf.2004.11.004
PubMed: 15777647
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Microarray and real-time RT-PCR analyses of differential human gene expression patterns induced by severe acute respiratory syndrome (SARS) coronavirus infection of Vero cells.</title><author><name sortKey="Leong, W F" sort="Leong, W F" uniqKey="Leong W" first="W F" last="Leong">W F Leong</name><affiliation><nlm:affiliation>Human Genome Laboratory, Department of Microbiology, Faculty of Medicine, National University of Singapore, Kent Ridge, Singapore 117597, Singapore.</nlm:affiliation></affiliation></author><author><name sortKey="Tan, H C" sort="Tan, H C" uniqKey="Tan H" first="H C" last="Tan">H C Tan</name></author><author><name sortKey="Ooi, E E" sort="Ooi, E E" uniqKey="Ooi E" first="E E" last="Ooi">E E Ooi</name></author><author><name sortKey="Koh, D R" sort="Koh, D R" uniqKey="Koh D" first="D R" last="Koh">D R Koh</name></author><author><name sortKey="Chow, Vincent T K" sort="Chow, Vincent T K" uniqKey="Chow V" first="Vincent T K" last="Chow">Vincent T K. Chow</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:15777647</idno><idno type="pmid">15777647</idno><idno type="doi">10.1016/j.micinf.2004.11.004</idno><idno type="wicri:Area/PubMed/Corpus">002836</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002836</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Microarray and real-time RT-PCR analyses of differential human gene expression patterns induced by severe acute respiratory syndrome (SARS) coronavirus infection of Vero cells.</title><author><name sortKey="Leong, W F" sort="Leong, W F" uniqKey="Leong W" first="W F" last="Leong">W F Leong</name><affiliation><nlm:affiliation>Human Genome Laboratory, Department of Microbiology, Faculty of Medicine, National University of Singapore, Kent Ridge, Singapore 117597, Singapore.</nlm:affiliation></affiliation></author><author><name sortKey="Tan, H C" sort="Tan, H C" uniqKey="Tan H" first="H C" last="Tan">H C Tan</name></author><author><name sortKey="Ooi, E E" sort="Ooi, E E" uniqKey="Ooi E" first="E E" last="Ooi">E E Ooi</name></author><author><name sortKey="Koh, D R" sort="Koh, D R" uniqKey="Koh D" first="D R" last="Koh">D R Koh</name></author><author><name sortKey="Chow, Vincent T K" sort="Chow, Vincent T K" uniqKey="Chow V" first="Vincent T K" last="Chow">Vincent T K. Chow</name></author></analytic><series><title level="j">Microbes and infection</title><idno type="ISSN">1286-4579</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Chlorocebus aethiops</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation</term><term>Genes, Viral (genetics)</term><term>Genes, Viral (physiology)</term><term>Humans</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>SARS Virus (physiology)</term><term>Severe Acute Respiratory Syndrome (metabolism)</term><term>Vero Cells</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Genes, Viral</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Genes, Viral</term><term>SARS Virus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Chlorocebus aethiops</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation</term><term>Humans</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Vero Cells</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Vero E6 African green monkey kidney cells are highly susceptible to infection with the newly emerging severe acute respiratory syndrome coronavirus (SARS-CoV), and they are permissive for rapid viral replication, with resultant cytopathic effects. We employed cDNA microarray analysis to characterize the cellular transcriptional responses of homologous human genes at 12 h post-infection. Seventy mRNA transcripts belonging to various functional classes exhibited significant alterations in gene expression. There was considerable induction of heat shock proteins that are crucial to the immune response mechanism. Modified levels of several transcripts involved in pro-inflammatory and anti-inflammatory processes exemplified the balance between opposing forces during SARS pathogenesis. Other genes displaying altered transcription included those associated with host translation, cellular metabolism, cell cycle, signal transduction, transcriptional regulation, protein trafficking, protein modulators, and cytoskeletal proteins. Alterations in the levels of several novel transcripts encoding hypothetical proteins and expressed sequence tags were also identified. In addition, transcription of apoptosis-related genes DENN and hIAP1 was upregulated in contrast to FAIM. Elevated Mx1 expression signified a strong host response to mediate antiviral resistance. Also expressed in infected cells was the C-terminal alternative splice variant of the p53 tumor suppressor gene encoding a modified truncated protein that can influence the activity of wild-type p53. We observed the interplay between various mechanisms to favor virus multiplication before full-blown apoptosis and the triggering of several pathways in host cells in an attempt to eliminate the pathogen. Microarray analysis identifies the critical host-pathogen interactions during SARS-CoV infection and provides new insights into the pathophysiology of SARS.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15777647</PMID><DateCompleted><Year>2005</Year><Month>07</Month><Day>05</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">1286-4579</ISSN><JournalIssue CitedMedium="Print"><Volume>7</Volume><Issue>2</Issue><PubDate><Year>2005</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Microbes and infection</Title><ISOAbbreviation>Microbes Infect.</ISOAbbreviation></Journal><ArticleTitle>Microarray and real-time RT-PCR analyses of differential human gene expression patterns induced by severe acute respiratory syndrome (SARS) coronavirus infection of Vero cells.</ArticleTitle><Pagination><MedlinePgn>248-59</MedlinePgn></Pagination><Abstract><AbstractText>Vero E6 African green monkey kidney cells are highly susceptible to infection with the newly emerging severe acute respiratory syndrome coronavirus (SARS-CoV), and they are permissive for rapid viral replication, with resultant cytopathic effects. We employed cDNA microarray analysis to characterize the cellular transcriptional responses of homologous human genes at 12 h post-infection. Seventy mRNA transcripts belonging to various functional classes exhibited significant alterations in gene expression. There was considerable induction of heat shock proteins that are crucial to the immune response mechanism. Modified levels of several transcripts involved in pro-inflammatory and anti-inflammatory processes exemplified the balance between opposing forces during SARS pathogenesis. Other genes displaying altered transcription included those associated with host translation, cellular metabolism, cell cycle, signal transduction, transcriptional regulation, protein trafficking, protein modulators, and cytoskeletal proteins. Alterations in the levels of several novel transcripts encoding hypothetical proteins and expressed sequence tags were also identified. In addition, transcription of apoptosis-related genes DENN and hIAP1 was upregulated in contrast to FAIM. Elevated Mx1 expression signified a strong host response to mediate antiviral resistance. Also expressed in infected cells was the C-terminal alternative splice variant of the p53 tumor suppressor gene encoding a modified truncated protein that can influence the activity of wild-type p53. We observed the interplay between various mechanisms to favor virus multiplication before full-blown apoptosis and the triggering of several pathways in host cells in an attempt to eliminate the pathogen. Microarray analysis identifies the critical host-pathogen interactions during SARS-CoV infection and provides new insights into the pathophysiology of SARS.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Leong</LastName><ForeName>W F</ForeName><Initials>WF</Initials><AffiliationInfo><Affiliation>Human Genome Laboratory, Department of Microbiology, Faculty of Medicine, National University of Singapore, Kent Ridge, Singapore 117597, Singapore.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>H C</ForeName><Initials>HC</Initials></Author><Author ValidYN="Y"><LastName>Ooi</LastName><ForeName>E E</ForeName><Initials>EE</Initials></Author><Author ValidYN="Y"><LastName>Koh</LastName><ForeName>D R</ForeName><Initials>DR</Initials></Author><Author ValidYN="Y"><LastName>Chow</LastName><ForeName>Vincent T K</ForeName><Initials>VT</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2005</Year><Month>01</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Microbes Infect</MedlineTA><NlmUniqueID>100883508</NlmUniqueID><ISSNLinking>1286-4579</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002522" MajorTopicYN="N">Chlorocebus aethiops</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="Y">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005814" MajorTopicYN="N">Genes, Viral</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014709" MajorTopicYN="N">Vero 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